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Non‐linear effects of blood pressure and glycosylated haemoglobin on progression of diabetic nephropathy
Author(s) -
Sawicki P. T.,
Bender R.,
Berger M.,
Mühlhauser I.
Publication year - 2000
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1046/j.1365-2796.2000.00622.x
Subject(s) - medicine , nephropathy , diabetic nephropathy , blood pressure , diabetes mellitus , logistic regression , risk factor , endocrinology
. Sawicki PT, Bender R, Berger M, Mühlhauser I (WHO‐Collaborating Centre for Diabetes, Heinrich‐Heine‐University of Düsseldorf, Germany). Non‐linear effects of blood pressure and glycosylated haemoglobin on progression of diabetic nephropathy. J Intern Med 2000; 247: 131–138. Objective. To describe the long‐term simultaneous impacts of blood pressure and glycosylated haemoglobin values on the risk of progression of diabetic nephropathy. Design. Prospective, multicentre, 6‐year follow‐up study. Setting. One reference centre (university department of internal medicine) and nine general hospitals. Subjects. A total of 601 type 1 diabetic patients on intensive insulin therapy with and without diabetic nephropathy. Main outcome measures. Progression of nephropathy was defined as change for the worse within five stages of nephropathy by at least one of these stages during the study period. By the use of logistic regression, the relationship between metabolic and blood pressure control and the risk of nephropathy progression was quantified. Results. The main determinants of nephropathy progression were glycosylated haemoglobin and blood pressure, which were both non‐linearly associated with the risk of progression. No significant threshold levels for any of the predictors of progression were identified. Conclusions. The results of this study underline the importance of optimizing metabolic and blood pressure control to arrest the progression of diabetic nephropathy without the evidence for a clinically relevant threshold effect.